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基于AMPK/GLUT4通路探究黄芩苷改善多囊卵巢综合征伴胰岛素抵抗的机制研究

To Explore the Mechanism of Baicalin in Improving Insulin Resistance in Polycystic Ovary Syndrome Based on the AMPK/GLUT4 Pathway
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摘要 目的:基于单磷酸腺苷酸活化蛋白激酶/葡萄糖转运蛋白4(Adenosine 5’-Monophosphate-Activated Protein Kinase/Glucose Transporter 4,AMPK/GLUT4)信号通路角度探索黄芩苷治疗多囊卵巢综合征伴胰岛素抵抗的机制。方法:将多囊卵巢综合征-胰岛素抵抗(Polycystic Ovary Syndrome-Insulin Resistance,PCOS-IR)造模成功小鼠随机分为模型组、地塞米松组、黄芩苷组3组,药物干预4周后,观察比较3组小鼠及空白对照组小鼠卵巢相关指标、血清空腹血糖(Fasting Blood Glucose,FBG)、空腹胰岛素(Fasting Insulin,FINS)以及卵巢组织中磷酯酰肌醇-3激酶(Phosphoester Inositol-3 Kinase,PI3K)、蛋白激酶B(Protein Kinase B,AKT)、GLUT4 mRNA表达水平。结果:与正常组小鼠相比,造模成功后小鼠卵巢最大横截面积、卵巢体积、卵巢指数、FBG水平、FINS水平均有显著上升,PI3K、AKT、GLUT4 mRNA表达水平显著下降(p<0.05),药物干预后,小鼠卵巢最大横截面积、卵巢体积、卵巢指数、FBG水平、FINS水平显著下降,PI3K、AKT、GLUT4 mRNA表达水平显著上升,黄芩苷组效果显著优于地塞米松组。结论:黄芩苷可以改善卵巢病理状态,上调PI3K/AKT/GLUT4信号通路蛋白表达水平,改善胰岛素抵抗及卵巢情况,为临床治疗多囊卵巢综合征伴胰岛素抵抗患者提供新思路。 Objective:To explore the mechanism of baicalin in the treatment of polycystic ovary syndrome with insulin resistance from the perspective of the Adenosine 5’-Monophosphate-Activated Protein Kinase/Glucose Transporter 4(AMPK/GLUT4)signaling pathway.Methods:The mice with successful Polycystic Ovary Syndrome-Insulin Resistance(PCOS-IR)modeling are randomly divided into three groups:the model group,the dexamethasone group and the baicalin group.After 4 weeks of drug intervention,observe and compare the ovaries related indicators,serum Fasting Blood Glucose(FBG),Fasting Insulin(FINS),Phosphoester Inositol-3 Kinase(PI3K)in ovarian tissue,Protein Kinase B(AKT)and GLUT4 mRNA of the three groups of mice and the blank control group mice.Results:Compare with the normal group of mice,after successful modeling,the maximum cross-sectional area of the ovary,ovarian volume,ovarian index,FBG level,and FINS level of the mice all significantly increase,while the expression levels of PI3K,AKT,and GLUT4 mRNA significantly decrease(p<0.05).After drug intervention,the maximum cross-sectional area of the ovaries,ovarian volume,ovarian index,FBG level and FINS level of mice decrease significantly,while the expression levels of PI3K,AKT and GLUT4 mRNA increase significantly.The effect of the baicalin group is significantly better than that of the dexamethasone group.Conclusion:Baicalin can improve the pathological state of the ovary,up-regulate the protein expression level of the PI3K/Akt/GLUT4 signaling pathway,improve insulin resistance and ovarian conditions,and provide new ideas for the clinical treatment of polycystic ovary syndrome-insulin resistance patients.
作者 徐藝文 王琰森 石炜灵 曾黎 刘美平 XU Yiwen;WANG Yansen;SHI Weiling;ZENG Li;LIU Meiping(Changsha Medical University,Changsha 410219,China)
机构地区 长沙医学院
出处 《生物化工》 2025年第5期100-103,共4页 Biological Chemical Engineering
基金 湖南省大学生创新创业训练计划项目(湘教通[2024]191号-5218)。
关键词 多囊卵巢综合征 胰岛素抵抗 信号通道 黄芩苷 polycystic ovary syndrome insulin resistance signal channel baicalin
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